Abstract
Exposure to arsenic through drinking water is a major public health problem affecting most countries, although the situation is particularly severe in low-income nations. The health consequences of chronic arsenic exposure include increased risk for various forms of cancer and numerous noncancer effects, including diabetes, skin diseases, chronic cough, and toxic effects on liver, kidney, cardiovascular system, and peripheral and central nervous systems. In recent years increasing reports of effects on fetal and child development have appeared. There seems to be a wide variation in susceptibility to arsenic toxicity, which is likely to be related to factors such as variation in arsenic metabolism, nutrition, host-related defense mechanisms, and genetic predisposition. The main mechanisms of arsenic-nutrition interactions include arsenic-induced oxidative stress, which requires nutrient-dependent defense systems, and arsenic metabolism (methylation) via 1-carbon metabolism, which requires methyl groups, folic acid, vitamin B-12, and betaine for the remethylation of homocysteine to methionine. An efficient first methylation step in combination with a slow second methylation step seems to be most critical from a toxicological point of view. A third mode of arsenic-nutrition interaction involves epigenetic effects and fetal programming via DNA methylation.
Highlights
Exposure to arsenic through drinking water is a major public health problem affecting most countries, the situation is severe in low-income nations
Premenopausal Bangladeshi women showed efficient methylation of arsenic [8], an observation made in East European population groups [94]. This may be related to the enhanced capacity to produce choline endogenously through de novo synthesis of phosphatidylcholine catalyzed by phosphatidylethanolamine N-methyltransferase (PEMT) in the female liver [93]
We evaluated the effects of measured biomarkers of folate, vitamin B-12, zinc, iron, and selenium status on arsenic metabolism in 442 women in early pregnancy, controlling for arsenic exposure, which was the main factor influencing arsenic methylation
Summary
DMA, dimethylarsinic acid; MMA, methylarsonic acid; PEMT, phosphatidylethanolamine N-methyltransferase; SAM, S-adenosylmethionine. Premenopausal Bangladeshi women showed efficient methylation of arsenic [8], an observation made in East European population groups [94] This may be related to the enhanced capacity to produce choline endogenously through de novo synthesis of phosphatidylcholine catalyzed by phosphatidylethanolamine N-methyltransferase (PEMT) in the female liver [93]. Low intakes of folic acid and vitamin B-12, which are involved in the remethylation of homocysteine to methionine, may decrease the efficiency of 1-carbon metabolism [35,36] Associations between these micronutrients and arsenic methylation have been reported in both experimental and epidemiological studies [90,95,96,97]. Estrogen induces the PEMT gene, which regulates the de novo synthesis of phosphatidylcholine, allowing pregnant women to make more of their needed choline, so critical for fetal development, endogenously [93,102]
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